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2017 ; 18
(5
): ä Nephropedia Template TP
gab.com Text
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English Wikipedia
Regulation of T(H)17 Cells and Associated Cytokines in Wound Healing, Tissue
Regeneration, and Carcinogenesis
#MMPMID28492497
Brockmann L
; Giannou AD
; Gagliani N
; Huber S
Int J Mol Sci
2017[May]; 18
(5
): ä PMID28492497
show ga
Wound healing is a crucial process which protects our body against permanent
damage and invasive infectious agents. Upon tissue damage, inflammation is an
early event which is orchestrated by a multitude of innate and adaptive immune
cell subsets including T(H)17 cells. T(H)17 cells and T(H)17 cell associated
cytokines can impact wound healing positively by clearing pathogens and
modulating mucosal surfaces and epithelial cells. Injury of the gut mucosa can
cause fast expansion of T(H)17 cells and their induction from naïve T cells
through Interleukin (IL)-6, TGF-?, and IL-1? signaling. T(H)17 cells produce
various cytokines, such as tumor necrosis factor (TNF)-?, IL-17, and IL-22, which
can promote cell survival and proliferation and thus tissue regeneration in
several organs including the skin, the intestine, and the liver. However, T(H)17
cells are also potentially pathogenic if not tightly controlled. Failure of these
control mechanisms can result in chronic inflammatory conditions, such as
Inflammatory Bowel Disease (IBD), and can ultimately promote carcinogenesis.
Therefore, there are several mechanisms which control T(H)17 cells. One control
mechanism is the regulation of T(H)17 cells via regulatory T cells and IL-10.
This mechanism is especially important in the intestine to terminate immune
responses and maintain homeostasis. Furthermore, T(H)17 cells have the potential
to convert from a pro-inflammatory phenotype to an anti-inflammatory phenotype by
changing their cytokine profile and acquiring IL-10 production, thereby limiting
their own pathological potential. Finally, IL-22, a signature cytokine of T(H)17
cells, can be controlled by an endogenous soluble inhibitory receptor,
Interleukin 22 binding protein (IL-22BP). During tissue injury, the production of
IL-22 by T(H)17 cells is upregulated in order to promote tissue regeneration. To
limit the regenerative program, which could promote carcinogenesis, IL-22BP is
upregulated during the later phase of regeneration in order to terminate the
effects of IL-22. This delicate balance secures the beneficial effects of IL-22
and prevents its potential pathogenicity. An important future goal is to
understand the precise mechanisms underlying the regulation of T(H)17 cells
during inflammation, wound healing, and carcinogenesis in order to design
targeted therapies for a variety of diseases including infections, cancer, and
immune mediated inflammatory disease.
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